title: Increased expression of heat shock protein 70 in chronic obstructive pulmonary disease.
abstract: BACKGROUND
  Heat shock protein 70 (HSP70) plays a critical role in the process of inflammation and innate immunity response under environmental stress.
  
  
  OBJECTIVE
  This study was to investigate HSP70 expression in the peripheral lung tissues of chronic obstructive pulmonary disease (COPD) patients and in human bronchial epithelial cells (16-HBE) exposed to cigarette smoke extract (CSE).
  
  
  METHODS
  Peripheral lung tissues were collected after lung cancer resection from 26 patients without COPD, 20 with mild COPD and 15 with advanced COPD, classified by lung function criteria. Among these cases, 37 were smokers and 24 non-smokers. Lung tissues were examined for histopathological changes and levels of HSP70 and IL-8. Cultured 16-HBE cells were stimulated with CSE in the absence or presence of HSP70 neutralizing antibody and the expressions of IL-8 and phospho-EGFR protein were determined.
  
  
  RESULTS
  Compared to patients without COPD, the levels of HSP70 and IL-8 were significantly increased in the lung tissues of COPD patients and positively correlated with the severity of the disease. The HSP70 expression was significantly higher in current smokers than that in non-smokers. Moreover, CSE-induced HSP70 significantly enhanced IL-8 production and EGFR phosphorylation in 16-HBE cells. The increases in IL-8 and phospho-EGFR were blocked by anti-HSP70 antibody.
  
  
  CONCLUSIONS
  Our study clarified that increased expression of HSP70 is closely related to COPD disease severity and smoking status. Extracellular HSP70 regulated chemokine productions and EGFR phosphorylation and plays an important role in the CSE-induced inflammatory and innate immunity responses in bronchial epithelia cells.
authors.affiliation: Division of Pulmonary Diseases, State Key Laboratory of Biotherapy of China and Department of Respiratory Medicine, West China Hospital of Sichuan University, Chengdu, Sichuan 610041, China.
authors.forename: Jiajia
authors.initials: J
authors.lastname: Dong
authors.forename: Lingli
authors.initials: L
authors.lastname: Guo
authors.forename: Zenglin
authors.initials: Z
authors.lastname: Liao
authors.forename: Mingke
authors.initials: M
authors.lastname: Zhang
authors.forename: Mingzhou
authors.initials: M
authors.lastname: Zhang
authors.forename: Tao
authors.initials: T
authors.lastname: Wang
authors.forename: Lei
authors.initials: L
authors.lastname: Chen
authors.forename: Dan
authors.initials: D
authors.lastname: Xu
authors.forename: Yulin
authors.initials: Y
authors.lastname: Feng
authors.forename: Fuqiang
authors.initials: F
authors.lastname: Wen
mesh_terms: D000368:Aged; D002460:Cell Line; D005260:Female; D018840:HSP70 Heat-Shock Proteins / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D016209:Interleukin-8 / Q000235:genetics / Q000378:metabolism; D008168:Lung / Q000378:metabolism / Q000473:pathology; D008297:Male; D008875:Middle Aged; D029424:Pulmonary Disease, Chronic Obstructive / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D012906:Smoke; D014026:Nicotiana
chemical_list: D018840:HSP70 Heat-Shock Proteins; D016209:Interleukin-8; D012906:Smoke
keywords: Airway inflammation; COPD; Cigarette smoke; EGFR; Heat shock protein; Interleukin-8